Abstract
BackgroundWalnut anthracnose induced by Colletotrichum gloeosporioides is a disastrous disease affecting walnut production. The resistance of walnut fruit to C. gloeosporioides is a highly complicated and genetically programmed process. However, the underlying mechanisms have not yet been elucidated.ResultsTo understand the molecular mechanism underlying the defense of walnut to C. gloeosporioides, we used RNA sequencing and label-free quantitation technologies to generate transcriptomic and proteomic profiles of tissues at various lifestyle transitions of C. gloeosporioides, including 0 hpi, pathological tissues at 24 hpi, 48 hpi, and 72 hpi, and distal uninoculated tissues at 120 hpi, in anthracnose-resistant F26 fruit bracts and anthracnose-susceptible F423 fruit bracts, which were defined through scanning electron microscopy. A total of 21,798 differentially expressed genes (DEGs) and 1929 differentially expressed proteins (DEPs) were identified in F26 vs. F423 at five time points, and the numbers of DEGs and DEPs were significantly higher in the early infection stage. Using pairwise comparisons and weighted gene co-expression network analysis of the transcriptome, we identified two modules significantly related to disease resistance and nine hub genes in the transcription expression gene networks. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of the DEGs and DEPs revealed that many genes were mainly related to immune response, plant hormone signal transduction, and secondary metabolites, and many DEPs were involved in carbon metabolism and photosynthesis. Correlation analysis between the transcriptome data and proteome data also showed that the consistency of the differential expression of the mRNA and corresponding proteins was relatively higher in the early stage of infection.ConclusionsCollectively, these results help elucidate the molecular response of walnut fruit to C. gloeosporioides and provide a basis for the genetic improvement of walnut disease resistance.
Highlights
Walnut anthracnose induced by Colletotrichum gloeosporioides is a disastrous disease affecting walnut production
The plant innate immune system mainly includes pathogenassociated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI), which rely on the MAPK cascade signaling network and molecular recognition to regulate the expression of corresponding genes, initiate a defense response, and produce systemic acquired resistance (SAR) through the salicylic acid (SA)-mediated signaling network [3, 4]
We showed that the lifestyle transitions of C. gloeosporioides in infected walnut fruits, and large amounts of differentially expressed genes (DEGs) and differentially expressed proteins (DEPs), were detected in F26 vs. F423 at different stages
Summary
Walnut anthracnose induced by Colletotrichum gloeosporioides is a disastrous disease affecting walnut production. The plant innate immune system mainly includes pathogenassociated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI), which rely on the MAPK cascade signaling network and molecular recognition to regulate the expression of corresponding genes, initiate a defense response, and produce systemic acquired resistance (SAR) through the salicylic acid (SA)-mediated signaling network [3, 4]. Numerous proteins encoded by resistance genes (R) act as intracellular immune receptors to recognize pathogen effector proteins and activate ETI, which in turn typically induces the local hypersensitive response (HR) cell death to restrict pathogen growth and propagation [8, 9]. The local HR can induce systemic acquired resistance (SAR) through the generation of mobile signals, accumulation of the defense hormone SA, and secretion of antimicrobial pathogenesis-related (PR) proteins
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